In the past year we have modified our immunohistochemical method for the localization of prolactin (PRL) binding sites in rat prostate tissue and increased its sensitivity 10 fold. Other immunohistochemcial studies are attempting to elucidate the "non-specific" Golgi localized staining in rat ventral prostate epithelial cells produced with rabbit anti-rat PRL (APRL) with the goal of obtaining a suitably specific PRL antiserum for the immunohistochemical localization of PRL bound in vivo by normal and neoplastic prostate tissue. In previous studies qualitative histologic evidence suggested that following castration there were regional variations in the rate of prostatic regression. Consequently, a statistically valid method was devised to estimate average epithelial cell height from photomicrographs of ventral, lateral and dorsal lobes of intact and castrated (1,2,4,8 days) rats. While ventral prostate epithelial cell heights declined 60% by 8 days post castration, those of dorsal and lateral lobes declined only about 20% at this time. The variations in castration-induced changes observed in rat prostate parallel changes in prolactin binding we reported previously. In other studies the growth rate of transplantable R3327 rat prostatic cancers was monitored. A spectrum of tumor growth rates were found ranging from very slow growing (doubling time, 38 days) to very rapidly growing (doubling time, 9 days). Histologic examination of selected tumor specimens representative of the spectrum of growth rates revealed no conspicuous differences in the degree of tumor alveolar development and interglandular neoplasia. In related experiments tumor growth rates were monitored prior to and following orchiectomy. Castration consistently retarded tumor growth although, as a rule, tumors continued to enlarge. Histologic examination of a small number of tumors from castrated hosts revealed large areas of necrosis adjacent to zones of apparently viable well-differentiated neoplasia.